Protective Effects of Pinostrobin on β-Amyloid-Induced Neurotoxicity in PC12 Cells

2012 ◽  
Vol 32 (8) ◽  
pp. 1223-1230 ◽  
Author(s):  
Yan-Fang Xian ◽  
Siu-Po Ip ◽  
Zhi-Xiu Lin ◽  
Qing-Qiu Mao ◽  
Zi-Ren Su ◽  
...  
2013 ◽  
Vol 38 (5) ◽  
pp. 951-960 ◽  
Author(s):  
Song-Zhi Kong ◽  
Yan-Fang Xian ◽  
Siu-Po Ip ◽  
Xiao-Ping Lai ◽  
Xu-Guang Shi ◽  
...  

2018 ◽  
Vol 103 ◽  
pp. 582-587 ◽  
Author(s):  
Nongnuch Singhrang ◽  
Chainarong Tocharus ◽  
Sarinthorn Thummayot ◽  
Manote Sutheerawattananonda ◽  
Jiraporn Tocharus

2004 ◽  
Vol 183 (3) ◽  
pp. 605-615 ◽  
Author(s):  
Botao Du ◽  
Masahide Ohmichi ◽  
Kazuhiro Takahashi ◽  
Jun Kawagoe ◽  
Chika Ohshima ◽  
...  

Although estrogen is known to protect against β-amyloid (Aβ)-induced neurotoxicity, the mechanisms responsible for this effect are only beginning to be elucidated. In addition, the effect of raloxifene on Aβ-induced neuro-toxicity remains unknown. Here we investigated whether raloxifene exhibits similar neuro-protective effects to estrogen against Aβ-induced neurotoxicity and the mechanism of the effects of these agents in PC12 cells transfected with the full-length human estrogen receptor (ER) α gene (PCER). Raloxifene, like 17β-estradiol (E2), significantly inhibited Aβ-induced apoptosis in PCER cells, but not in a control line of cells transfected with vector DNA alone (PCCON). Since telomerase activity, the level of which is modulated by regulation of telomerase catalytic subunit (TERT) at both the transcriptional and post-transcriptional levels, is known to be involved in suppressing apoptosis in neurons, we examined the effect of E2 and raloxifene on telomerase activity. Although both E2 and raloxifene induced telomerase activity in PCER cells, but not in PCCON cells, treated with Aβ, they had no effect on the level of TERT expression. These results suggest that neither E2 nor raloxifene affects the telomerase activity at the transcriptional level. We therefore studied the mechanism by which E2 and raloxifene induce the telomerase activity at the post-transcriptional level. Both E2 and raloxifene induced the phosphorylation of Akt, and pre-treatment with a phosphatidylinositol 3-kinase inhibitor, LY294002, attenuated both E2− and raloxifene-induced activation of the telomerase activity. Moreover, both E2 and raloxifene induced both the phosphorylation of TERT at a putative Akt phosphorylation site and the association of nuclear factor κB with TERT. Our findings suggest that and raloxifene exert neuroprotective effects by E2 telomerase activation via a post-transcriptional cascade in an experimental model relevant to Alzheimer’s disease.


Molecules ◽  
2012 ◽  
Vol 17 (9) ◽  
pp. 10831-10845 ◽  
Author(s):  
Seung-Young Hong ◽  
Woo-Sik Jeong ◽  
Mira Jun

2013 ◽  
Vol 11 (8) ◽  
pp. 1030-1037 ◽  
Author(s):  
Tao Luo ◽  
Wei Jiang ◽  
Yan Kong ◽  
Sheng Li ◽  
Feng He ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Yunkyoung Lee ◽  
Hee-Sook Jun ◽  
Yoon Sin Oh

The extract of Psoralea corylifolia seeds (PCE) has been widely used as a herbal medicine because of its beneficial effect on human health. In this study, we investigated the protective effects and molecular mechanisms of PCE on palmitate- (PA-) induced toxicity in PC12 cells, a neuron-like cell line. PCE significantly increased cell viability in PA-treated PC12 cells and showed antiapoptotic effects, as evidenced by decreased expression of cleaved caspase-3, cleaved poly(ADP-ribose) polymerase, and bax protein as well as increased expression of bcl-2 protein. In addition, PCE treatment reduced PA-induced reactive oxygen species production and upregulated mRNA levels of antioxidant genes such as nuclear factor (erythroid-derived 2)-like 2 and heme oxygenase 1. Moreover, PCE treatment recovered the expression of autophagy marker genes such as beclin-1 and p62, which was decreased by PA treatment. Treatment with isopsoralen, one of the major components of PCE extract, also recovered the expression of autophagy marker genes and reduced PA-induced apoptosis. In conclusion, PCE exerts protective effects against lipotoxicity via its antioxidant function, and this effect is mediated by activation of autophagy. PCE might be a potential pharmacological agent to protect against neuronal cell injury caused by oxidative stress or lipotoxicity.


2021 ◽  
Vol 26 ◽  
pp. 101020
Author(s):  
Gregory J. Tsay ◽  
Yu-Ta Lin ◽  
Chia-Hong Hsu ◽  
Feng-Yao Tang ◽  
Yueh-Hsiung Kuo ◽  
...  

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